Traumatic neuroma of the mandible: a case report with spontaneous remission

Traumatic neuroma is a well-known disorder involving peripheral nerves, which occurs following trauma or sur - gery. The lesion develops most commonly in the soft tissues of the mental foramen area, lower lip and tongue. Intra- osseous lesions arising in jawbones are very uncommon. In this paper, we report a new case of an intra-osseous traumatic neuroma, discovered incidentally on a panoramic radiograph obtained for orthodontic documentation. In addition, the case herein described developed spontaneous remission, a situation not previously reported in the literature. Finally, we discuss relevant demographic, clinical, microscopic, immunohistochemical and treatment aspects of traumatic neuromas

Amplification of the Angiogenic Signal through the Activation of the TSC/mTOR/HIF Axis by the KSHV vGPCR in Kaposi's Sarcoma

Background: Kaposi’s sarcoma (KS) is a vascular neoplasm characterized by the dysregulated expression of angiogenic and inflammatory cytokines. The driving force of the KS lesion, the KSHV-infected spindle cell, secretes elevated levels of vascular endothelial growth factor (VEGF), essential for KS development. However, the origin of VEGF in this tumor remains unclear. Methodology/Principal Findings: Here we report that the KSHV G protein-coupled receptor (vGPCR) upregulates VEGF in KS through an intricate paracrine mechanism. The cytokines secreted by the few vGPCR-expressing tumor cells activate in neighboring cells multiple pathways (including AKT, ERK, p38 and IKK$\beta$) that, in turn, converge on TSC1/2, promoting mTOR activation, HIF upregulation, and VEGF secretion. Conditioned media from vGPCR-expressing cells lead to an mTORdependent increase in HIF-1$\alpha$ and HIF-2$\alpha$ protein levels and VEGF upregulation. In a mouse allograft model for KS, specific inhibition of the paracrine activation of mTOR in non-vGPCR-expressing cells was sufficient to inhibit HIF upregulation in these cells, and abolished the ability of the vGPCR-expressing cells to promote tumor formation $in$ $vivo$. Similarly, pharmacologic inhibition of HIF in this model blocked VEGF secretion and also lead to tumor regression. Conclusions/Significance: Our findings provide a compelling explanation for how the few tumor cells expressing vGPCR can contribute to the dramatic amplification of VEGF secretion in KS, and further provide a molecular mechanism for how cytokine dysregulation in KS fuels angiogenesis and tumor development. These data further suggest that activation of HIF by vGPCR may be a vulnerable target for the treatment of patients with KS

Expression of midkine in ameloblastomas and its correlation with clinicopathologic parameters

ObjectiveMidkine (MK) is a heparin-binding growth factor that is overexpressed in various human cancers. The aim of this study was to investigate the expression of MK in ameloblastomas and correlate the results with clinicopathologic parameters.Study DesignCases of ameloblastoma seen between 1999 and 2010 were identified. Clinical information was collected regarding age, gender, race, and location of tumor. Cases were classified as solid/multicystic, unicystic, and peripheral. The expression of midkine was assessed using immunohistochemistry. A significant difference was considered present at P < 0.05.ResultsA total of 34 cases of ameloblastoma and 4 cases of ameloblastic carcinomas were identified. MK was expressed in 67% of lesions (23.5% weak expression; 14.7% moderate expression; 29.4% strong expression). A significant difference was seen between solid/multicystic and unicystic lesions.ConclusionsMK is expressed in the majority of ameloblastomas, suggesting a role of the protein in the tumor's development, progression, and behavior